Medial medullary infarct aggravates central poststroke pain caused by previous lateral medullary infarct

Although the pathogenesis of central poststroke pain (CPSP) remains obscure, interactions between the spinothalamic tract and lemniscal sensory tract may be involved in its pathogenic mechanism.

A patient developed lateral medullary infarction, which produced contralateral spinothalamic sensory deficits and subsequent CPSP. The CPSP gradually improved until the development of ipsilateral medial medullary infarction 26 months later, which was associated with mild hemiparesis and lemniscal sensory deficits. The ipsilateral medial medullary infarction immediately aggravated the CPSP to its previous level.

This observation has implications regarding the pathogenesis of CPSP. CPSP may be related to hyperexcitation of the spinothalamic pathway by the reticulothalamic system, which in turn is modulated by the medial lemniscus pathway.